Palmitoylation of influenza virus proteins

2013 ◽  
Vol 41 (1) ◽  
pp. 50-55 ◽  
Author(s):  
Michael Veit ◽  
Marina V. Serebryakova ◽  
Larisa V. Kordyukova
Keyword(s):  
Influenza Viruses ◽  
Spike Protein ◽  
Proton Channel ◽  
Membrane Rafts ◽  
Target Cells ◽  
Virus Particles ◽  
Functional Consequences ◽  
Infected Cells ◽  
Fatty Acid Species ◽  
Acylated Proteins

Influenza viruses contain two palmitoylated (S-acylated) proteins: the major spike protein HA (haemagglutinin) and the proton-channel M2. The present review describes the fundamental biochemistry of palmitoylation of HA: the location of palmitoylation sites and the fatty acid species bound to HA. Finally, the functional consequences of palmitoylation of HA and M2 are discussed regarding association with membrane rafts, entry of viruses into target cells by HA-mediated membrane fusion as well as the release of newly assembled virus particles from infected cells.

scholarly journals Antibody to influenza virus matrix protein detects a common antigen on the surface of cells infected with type A influenza viruses.

1977 ◽  
Vol 146 (3) ◽  
pp. 690-697 ◽  
Author(s):  
W E Biddison ◽  
P C Doherty ◽  
R G Webster
Keyword(s):  
Influenza Virus ◽  
Matrix Protein ◽  
Type A ◽  
Cross Reactivity ◽  
T Cell Response ◽  
Influenza Viruses ◽  
Cytotoxic T Cell ◽  
Target Cells ◽  
Common Antigen ◽  
Infected Cells

Antisera to the type-specific internal influenza virus matrix (M) protein of a type A influenza virus were produced in goats. In the presence of complement, anti-M serum was cytotoxic for target cells which were infected with a variety of serologically distinct type A influenza viruses, but did not react with type B influenza virus-infected cells. Absorption experiments indicated that anti-M serum detected a common antigen(s) on the surface of type A-infected cells. This serological cross-reactivity parallels the cross-reactivity observed for the cytotoxic T-cell response to type A viruses.

Global properties of nonlinear humoral immunity viral infection models

2015 ◽  
Vol 08 (05) ◽  
pp. 1550058 ◽  
Author(s):  
A. M. Elaiw ◽  
N. H. AlShamrani
Keyword(s):  
Viral Infection ◽  
Humoral Immunity ◽  
Nonlinear Models ◽  
Removal Rate ◽  
Lyapunov Theory ◽  
Target Cells ◽  
Global Dynamics ◽  
Virus Particles ◽  
Latently Infected ◽  
Infected Cells

In this paper, we consider two nonlinear models for viral infection with humoral immunity. The first model contains four compartments; uninfected target cells, actively infected cells, free virus particles and B cells. The second model is a modification of the first one by including the latently infected cells. The incidence rate, removal rate of infected cells, production rate of viruses and the latent-to-active conversion rate are given by more general nonlinear functions. We have established a set of conditions on these general functions and determined two threshold parameters for each model which are sufficient to determine the global dynamics of the models. The global asymptotic stability of all equilibria of the models has been proven by using Lyapunov theory and applying LaSalle's invariance principle. We have performed some numerical simulations for the models with specific forms of the general functions. We have shown that, the numerical results are consistent with the theoretical results.

scholarly journals Stability Analysis of Mathematical Modeling of Interaction between Target Cells and COVID-19 Infected Cells

2021 ◽  
Vol 10 (2) ◽  
pp. 123-127
Author(s):  
Sugiyanto Sugiyanto ◽  
Mansoor Abdul Hamid ◽  
Alya Adianta ◽  
Hanny Puspha Jayanti ◽  
Muhammad Ja'far Luthfi
Keyword(s):  
Mathematical Model ◽  
Stability Analysis ◽  
Target Cells ◽  
Effective Surface ◽  
Cycle Number ◽  
Virus Particles ◽  
Opposite Sequence ◽  
Infected Cells ◽  
The Stability ◽  
The One

The stability analysis in this mathematical model was related to the infection of the Coronavirus Disease 2019 (Covid-19). In this mathematical model there were two balance points, namely the point of balance free from Covid-19 and the one infected with Covid-19. The stability of the equilibrium point was influenced by all parameters, i.e. target cells die during each cycle, number of target cells at  = 0, target cells infected during each cycle based on virion unit density, effective surface area of the network, the ratio of the number of virus particles to the number of virions, infected cells die during each cycle, the number of virus particles produced by each infected cell during each cycle, and virus particles die during each cycle. In the simulation model, immunity is divided into high, medium and low immunity. For high, moderate and low immunity, respectively, the highest number of target cells is in high, medium and low immunity, whereas for the number of infected cells and the number of Covid-19, it is in the opposite sequence of the number of target cells.

scholarly journals Maoto, a Traditional Japanese Herbal Medicine, Inhibits Uncoating of Influenza Virus

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Shinta Masui ◽  
Shigeki Nabeshima ◽  
Kazuhiko Ajisaka ◽  
Kei Yamauchi ◽  
Ryota Itoh ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Herbal Medicine ◽  
A549 Cells ◽  
Virus Titer ◽  
Influenza Viruses ◽  
Viral Rna ◽  
Virus Particles ◽  
Endosomal Acidification ◽  
Infected Cells ◽  
Virological Efficacy

We previously reported in randomized controlled trials that maoto, a traditional herbal medicine, showed clinical and virological efficacy for seasonal influenza. In this study, a culturing system for influenza was used to test the effect of maoto. A549 cells in the culture were infected with influenza virus A (PR8) and followed after treatment with maoto; the virus titers in the culture supernatant, intracellular viral proteins, and viral RNA were determined. When infected cells were cultured with maoto for 24 hr, the virus titer and protein were significantly reduced compared with medium only. Other subtypes, A/H3N2, H1N1pdm, and B, were also inhibited by maoto. Proliferation of viral RNA in a 6 hr culture was inhibited by maoto in the early phase, especially in the first 30 min. Focusing on the entry step of the influenza virus, we found that endosomal pH, regulated by vacuolar-type H+ATPase (V-ATPase) located in the membrane, was increased when treated with maoto. We also found that uncoating of influenza viruses was also inhibited by maoto, resulting in the increase of the number of virus particles in endosomes. These results strongly suggest that the inhibition of endosomal acidification by maoto results in blocking influenza virus entry to cytoplasm, probably through the inhibition of V-ATPase. The present study provides evidence that supports the clinical use of maoto for the treatment of influenza.

scholarly journals Efficient isolation and propagation of human immunodeficiency virus on recombinant colony-stimulating factor 1-treated monocytes.

1988 ◽  
Vol 167 (4) ◽  
pp. 1428-1441 ◽  
Author(s):  
H E Gendelman ◽  
J M Orenstein ◽  
M A Martin ◽  
C Ferrua ◽  
R Mitra ◽  
...  
Keyword(s):  
Cell Formation ◽  
Reverse Transcriptase Activity ◽  
Target Cells ◽  
Virus Particles ◽  
Hiv Rna ◽  
Macrophage Tropism ◽  
Giant Cell Formation ◽  
Hiv Antigen ◽  
Infected Cells ◽  
T Cell Lines

Monocytes were maintained in tissue culture for greater than 3 mo in media supplemented with rCSF-1. These cultures provided susceptible target cells for isolation and propagation of virus from PBMC of HIV-infected patients. HIV isolated into monocytes readily infected other rCSF-1-treated monocytes but only inefficiently infected PHA-stimulated lymphoblasts. Similarly, laboratory HIV strains passaged in T cell lines or virus isolated from patients' leukocytes into PHA-stimulated lymphoblasts inefficiently infected rCSF-1-treated monocytes. Persistent, low-level virion production was detected in macrophage culture fluids by reverse transcriptase activity or HIV antigen capture through 6-7 wk. Marked changes in cell morphology with cell death, syncytia, and giant cell formation were observed in monocyte cultures 2 wk after infection, but at 4-6 wk, all cells appeared morphologically normal. However, the frequency of infected cells in these cultures at 6 wk was 60-90% as quantified by in situ hybridization with HIV RNA probes or by immunofluorescence with AIDS patients' sera. Ultrastructural analysis by EM also showed a high frequency of infected cells; virtually all HIV budded into and accumulated within cytoplasmic vacuoles and virus particles were only infrequently associated with the plasma membrane. Retention of virus within macrophages and the macrophage tropism of HIV variants may explain mechanisms of both virus persistence and dissemination during disease.

scholarly journals Directional Spread of Surface-Associated Retroviruses Regulated by Differential Virus-Cell Interactions

2010 ◽  
Vol 84 (7) ◽  
pp. 3248-3258 ◽  
Author(s):  
Nathan M. Sherer ◽  
Jing Jin ◽  
Walther Mothes
Keyword(s):  
Cell Surface ◽  
Viral Infections ◽  
Leukemia Virus ◽  
Cell Interactions ◽  
Target Cells ◽  
Specific Cell ◽  
Cell Periphery ◽  
Surface Receptors ◽  
Virus Particles ◽  
Infected Cells

ABSTRACT The spread of viral infections involves the directional progression of virus particles from infected cells to uninfected target cells. Prior to entry, the binding of virus particles to specific cell surface receptors can trigger virus surfing, an actin-dependent lateral transport of viruses toward the cell body (M. J. Lehmann et al., J. Cell Biol. 170:317-325, 2005; M. Schelhaas, et al., PLoS Pathog. 4:e1000148, 2008; J. L. Smith, D. S. Lidke, and M. A. Ozbun, Virology 381:16-21, 2008). Here, we have used live-cell imaging to demonstrate that for cells chronically infected with the gammaretrovirus murine leukemia virus in which receptor has been downregulated, a significant portion of completely assembled virus particles are not immediately released into the supernatant but retain long-term association with the cell surface. Retention can be attributed, at least in part, to nonspecific particle attachment to cell surface glycosylaminoglycans. In contrast to virus surfing, viruses retained at the surface of infected cells undergo a lateral motility that is random and actin independent. This diffusive motility can be abruptly halted and converted into inward surfing after treatment with Polybrene, a soluble cation that increases virus-cell adsorption. In the absence of Polybrene, particle diffusion allows for an outward flow of viruses to the infected cell periphery. Peripheral particles are readily captured by and transmitted to neighboring uninfected target cells in a directional fashion. These data demonstrate a surface-based mechanism for the directional spread of viruses regulated by differential virus-cell interactions.

Further Observations on the Virus of Epizootic Diarrhea of Infant Mice. An Electron Microscopic Study

1967 ◽  
Vol 25 ◽  
pp. 110-111
Author(s):  
W. G. Banfield ◽  
G. Kasnic ◽  
J. H. Blackwell
Keyword(s):  
Electron Microscope ◽  
Infected Cell ◽  
Microscopic Study ◽  
Intestinal Epithelium ◽  
Ultrastructural Study ◽  
Osmium Tetroxide ◽  
Lead Citrate ◽  
Electron Microscopic ◽  
Virus Particles ◽  
Infected Cells

An ultrastructural study of the intestinal epithelium of mice infected with the agent of epizootic diarrhea of infant mice (EDIM virus) was first performed by Adams and Kraft. We have extended their observations and have found developmental forms of the virus and associated structures not reported by them.Three-day-old NLM strain mice were infected with EDIM virus and killed 48 to 168 hours later. Specimens of bowel were fixed in glutaraldehyde, post fixed in osmium tetroxide and embedded in epon. Sections were stained with uranyl magnesium acetate followed by lead citrate and examined in an updated RCA EMU-3F electron microscope.The cells containing virus particles (infected) are at the tips of the villi and occur throughout the intestine from duodenum through colon. All developmental forms of the virus are present from 48 to 168 hours after infection. Figure 1 is of cells without virus particles and figure 2 is of an infected cell. The nucleus and cytoplasm of the infected cells appear clearer than the cells without virus particles.

Studies of a Defective Measles Virus

1968 ◽  
Vol 26 ◽  
pp. 208-209
Author(s):  
R. M. McCombs ◽  
M. Benyesh-Melnick ◽  
J. P. Brunschwig
Keyword(s):  
Inclusion Bodies ◽  
Measles Virus ◽  
Giant Cells ◽  
Helical Structures ◽  
Thin Sections ◽  
Virus Particles ◽  
Extracellular Virus ◽  
Culture Cells ◽  
Infected Cells ◽  
Eosinophilic Inclusions

Measles virus is an agent that is capable of replicating in a number of different culture cells and generally causes the formation of multinucleated giant cells. As a result of infection, virus is released from the cells into the culture fluids and reinfection can be initiated by this cell-free virus. The extracellular virus has been examined by negative staining with phosphotungstic acid and has been shown to be a rather pleomorphic particle with a diameter of about 140 mμ. However, no such virus particles have been detected in thin sections of the infected cells. Rather, the only virus-induced structures present in the giant cells are eosinophilic inclusions (intracytoplasmic or intranuclear). These inclusion bodies have been shown to contain helical structures, resembling the nucleocapsid observed in negatively stained preparations.

scholarly journals Human plasmacytoid dendritic cells mount a distinct antiviral response to virus-infected cells

2021 ◽  
Vol 6 (58) ◽  
pp. eabc7302
Author(s):  
Tae Jin Yun ◽  
Suzu Igarashi ◽  
Haoquan Zhao ◽  
Oriana A. Perez ◽  
Marcus R. Pereira ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Virus Detection ◽  
Plasmacytoid Dendritic Cells ◽  
Lung Epithelial Cells ◽  
Live Cells ◽  
Type I ◽  
Antiviral Immune Response ◽  
Lung Epithelial ◽  
Functional Consequences ◽  
Infected Cells

Plasmacytoid dendritic cells (pDCs) can rapidly produce interferons and other soluble factors in response to extracellular viruses or virus mimics such as CpG-containing DNA. pDCs can also recognize live cells infected with certain RNA viruses, but the relevance and functional consequences of such recognition remain unclear. We studied the response of primary DCs to the prototypical persistent DNA virus, human cytomegalovirus (CMV). Human pDCs produced high amounts of type I interferon (IFN-I) when incubated with live CMV-infected fibroblasts but not with free CMV; the response involved integrin-mediated adhesion, transfer of DNA-containing virions to pDCs, and the recognition of DNA through TLR9. Compared with transient polyfunctional responses to CpG or free influenza virus, pDC response to CMV-infected cells was long-lasting, dominated by the production of IFN-I and IFN-III, and lacked diversification into functionally distinct populations. Similarly, pDC activation by influenza-infected lung epithelial cells was highly efficient, prolonged, and dominated by interferon production. Prolonged pDC activation by CMV-infected cells facilitated the activation of natural killer cells critical for CMV control. Last, patients with CMV viremia harbored phenotypically activated pDCs and increased circulating IFN-I and IFN-III. Thus, recognition of live infected cells is a mechanism of virus detection by pDCs that elicits a unique antiviral immune response.

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